This is a case of a 56-year-old male with an unremarkable past psychiatric and family history. He was previously healthy except for having untreated hypertension, dyslipidemia, and being a tobacco chewer. He was married with children, and was a semi-retired business owner.

His initial presentation to the emergency occurred after a sudden onset of severe headache, dizziness, nausea, vomiting, blurry vision, slurred speech, and ataxia. His initial CT scan was inconclusive but a subsequent MRI later the same day demonstrated extensive acute bilateral cerebellar infarcts with some involvement of the midbrain colliculi and superior cerebellar peduncles (Fig. 1). A CT angiogram of the head and neck performed on the same day indicated an intracranial left vertebral artery dissection with embolus to the distal basilar artery extending into the P1 segment of the left posterior cerebral artery. Bilateral SCA territory infarcts were indicated by patchy areas of hypoattenuation within the bilateral cerebellar hemispheres as well as the inferior right and bilateral superior cerebellar lobes (Fig. 1).

The patient had otherwise unremarkable findings from medical investigations including a normal transthoracic echocardiogram. During his admission to the stroke neurology unit, the patient suffered from ongoing significant ataxia, dysarthria, scanning speech, motor dysmetria, and mild diplopia. He required a temporary nasogastric tube feed and subsequent insertion of a peg tube for 3 months due to dysphagia. There was mild right-sided hemisensory impairment to sharp touch and temperature, which resolved after 4 months. His other neurological symptoms gradually improved but did not completely resolve over his nearly 5-month admission to hospital. Dysmetria and ataxia were most resistant to rehabilitation.

Approximately 2 days into his admission, records indicated that the patient began experiencing hallucinations and was thought to be “confused.” The patient described seeing cameras and police in his room at night. He expressed delusions such as “Russians are coming to get me”, “police were stealing people away at night”, and became suspicious that his wife was committing adultery. The patient’s perceptual disturbances were more pronounced at night. Extensive laboratory investigations were performed along with repeat head CT scans and a review of his medications -- all results were non-indicative for delirium. After 3 weeks, his symptoms persisted despite maintaining orientation in all three spheres. The consulting psychiatrist diagnosed the patient with “psychotic disorder due to stroke” based on the observation that the patient suffered from delusions and hallucinations with a lack of insight. He was started on 2.5 mg Olanzapine at night. Consequently, the patient reportedly slept more at night although accounts of his paranoid delusions and agitation persisted. The anxiety associated with his perceptual disturbances appeared to diminish over the next 3 weeks until discharge.

The patient was transferred to an inpatient stroke rehabilitation hospital for another 3 months and Olanzapine was discontinued on admission as per his request. Psychiatry was re-consulted as the patient expressed ongoing fears of being harmed by intruders in the hospital and complained of hearing people being shot at night, which affected his sleep. He believed that SWAT members were consistently lurking in the hallways. He lacked insight about his fixed ideas and endorsed his beliefs throughout the day to his wife and staff. His affect was flat and minimally reactive during assessments. His speech was slow and monotone but he could express himself coherently otherwise. Other than anxiety related to his delusions the patient denied experiencing problems with depression. A repeat brain MRI disclosed no new findings. The patient was diagnosed with a “persistent post-stroke psychosis”. He agreed to restarting Olanzapine and the dose was gradually increased to 5 mg in the evenings. Same as before, the patient’s delusions and hallucinations did not subside but he reported significantly less anxiety about his delusions and had better sleep.

On the cognitive level, based on formal tests involving the Brixton Spatial Anticipation Test, Indendent Living Scale, Repeatable Battery for the Assessment of Neuropsychological Status, and Weschler Memory Scale (WMS-III: Spatial Span Subtest), the patient was impaired in the following domains: divided attention/multitasking (mild impairment), visual-spatial working memory (mild impairment), and immediate and delayed memory for verbal information (mild to moderate impairment). Novel problem-solving ability was in the low average range. Family members and health care staff commented that the patient showed impulsivity in behavior resulting in unsafe transfers and having a “shorter fuse.” In contrast, the patient was found to have above average language and fine visual-spatial judgment of angles and distances. Auditory working memory fell within normal limits.

The patient was scheduled for a follow-up appointment with outpatient psychiatry in one month’s time but he did not attend. He was subsequently lost to follow-up.

Our patient had partial response to Olanzapine on both 2.5 and 5 mg evening doses. Mainly sleep and anxiety were improved but abatement of psychotic symptoms was questionable. The dose may have been inadequate or perhaps Olanzapine’s receptor profile was inadequate for the region of pathology. To the best of our knowledge, there is no consensus on preferred pharmacological treatment of psychotic symptoms secondary to cerebellar lesions. There are limited case reports on treatment, however one case reported success with a combination of Clozapine and Valproate [10]. Another article reported success in treating a patient’s depressive and psychotic symptoms with Fluoxetine and Risperidone [11].

Written informed consent was obtained from the patient for the publication of this report and any accompanying images.